In our earlier studies, we have shown that a cross-reactive idiotype (Id-1) was associated with the anti-Group A streptococcal carbohydrate (SACHO) antibodies produced by a high percentage of rats of several inbred strains. These studies were, also, designed to carefully characterize Id-1 in terms of localization of the idiotypic determinants on H-and/or L-chains. The major objective of this proposed research will be to determine the consequence(s) of maternally-derived idiotype and/or anti-idiotype on the immune repetoire of progeny. Idiotypes and anti-idiotypes may be transferred to progeny prior to birth via the placenta and/or after birth by means of colostrum and milk. These maternal "factors", responsible for altering progeny immune responsiveness to antigen may be soluble protein and/or protein associated with the surface of lymphocytes. Depending upon the immune reactivity of different females, under certain experimental conditions we may observe suppression of the progeny Id-1 expression, whereas under other conditions an enhancement of the Id-1 and/or anti-SACHO response may be observed. The duration of these effects may also be expected to vary depending upon the underlying mechanism involved. An understanding of the maternal-fetal interchange, which normally occurs during gestation and neonatal development should provide a very sensitive means for studying GASV induced idiotype-anti-idiotype interactions in vivo since fetal and newborn lymphocytes are very susceptible to modulating influences. An important outcome of defining and understanding the mechanism of maternal-fetal idiotype interactions concerns its direct applicability to immunological engineering. Idiotype suppression provides a selective mechanism for modulating the immune system especially as related to tissue transplantation, allergy, and autoimmunity. Idiotype-anti-idiotype enhancement could allow the selective expansion of antibody-producing clones of a particular class, subclass and antigen specificity.